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Inorganic particles dispersed in the polymer matrix can enhance the strength of polymers. In this paper, 3-Glycidyloxypropyltrimethoxysilane (KH560) and 2-Amino-1,3-propanediol were used to surface modify Zirconium dioxide (ZrO2) to prepare modified Zirconium dioxide (ZrO2), denoted as ZrO2-g. The modified ZrO2-g was characterized by Fourier transform infrared (FTIR) spectroscopy and nuclear magnetic hydrogen (1HNMR) spectroscopy, and the results showed that the modification was successful. Then the PBAT/ZrO2-g composites were synthesized by grafting ZrO2-g into poly (butylene adipate-co-terephthalate) (PBAT) molecular chain segments using in situ copolymerization. The results showed that ZrO2-g acted as a nucleating agent and improved the crystallinity of poly (butylene adipate-co-terephthalate) (PBAT). The rheological behavior analysis showed that the composite viscosity, storage modulus and loss modulus of PBAT/ZrO2-g composites were improved compared to PBAT. The ZrO2-g content had a significant effect on the tensile properties of the composites, and the composites had the highest tensile strength and elongation at break when the ZrO2-g content was 1% wt, reaching 23.27 MPa and 888.89%, respectively, which were increased by 60% and 38%, respectively, compared with PBAT. When the content of ZrO2-g exceeds 1.5 wt%, aggregation phenomenon occurs, which rather reduces the performance of the composites. Meanwhile, the thermal stability of the composites decreases with the increase of ZrO2-g incorporation. [ABSTRACT FROM AUTHOR]

Comprehensive Summary: Artemiprincepsolides A—F (1—6) were isolated from Artemisia princeps guided by bioactivity and elucidated by comprehensive spectral data and ECD calculation. Compounds 1—3 represented the first connecting model of germacrane‐guaiane hetero‐dimeric adducts, and compounds 4—6 were eudesmane‐guaiane hetero‐coupled sesquiterpenoid dimers, meanwhile, all these were presumably formed by Diels‐Alder cycloaddition. Compounds 1—6 were evaluated for their hepatomatic cytotoxicity on three hepatoma cell lines, and demonstrated cytotoxicity with IC50 values in the range of 5.0—67.3 μmol/L. Interestingly, compound 1 manifested significant cytotoxicity against HepG2, Huh7, and SK‐Hep‐1 cells with IC50 values of 9.9, 9.2, and 5.0 μmol/L, which were almost equivalent to the positive control, sorafenib. Flow cytometry data and Western blot assays revealed the most active compound 1 dose‐dependently inhibited cell migration and invasion, and significantly induced HepG2 cells arrest in G2/M phase by downregulating proteins pcdc2 and upregulating the level of protein CyclinB1; and induced apoptosis by downregulating of Bcl‐2 expression and upregulating Bax level. [ABSTRACT FROM AUTHOR]

Comprehensive Summary: 17 new guaiane‐type sesquiterpenoid dimers (GSDs), artemzhongdianolides B1—B17 (1—17), were isolated from Artemisia zhongdianensis under the guidance of bioassay, and elucidated by spectral analyses (HRESIMS, 1D and 2D NMR, IR, ECD). The absolute configuration of compounds 1, 3, 7, 9, 10, and 13 was determined by single‐crystal X‐ray diffraction analyses. Structurally, artemzhongdianolides B1 (1) and B2 (2) were the first example of the GSDs fused via a C‐13/C‐13' single bond, and artemzhongdianolides B3—B17 were [4 + 2] Diels–Alder adducts of two monomeric guaianolides. Most of the compounds showed antihepatoma cytotoxicity with IC50 values ranging from 9.9 to 170.1 μmol/L. Importantly, artemzhongdianolide B9 (9) was the most active one against three hepatoma cell lines with IC50 values of 13.1 μmol/L (HepG2), 19.5 μmol/L (Huh7), and 19.5 μmol/L (SK‐Hep‐1), and dose‐dependently inhibited cell migration and invasion, induced G1 cell cycle arrest and cell apoptosis in HepG2 cells. Compound 9 might suppress HepG2 cells via affecting the p38MAPK signaling pathway suggested by machine learning approach, and significantly upregulated expression of phosphorylated p38 validated by Western blot assay. [ABSTRACT FROM AUTHOR]

(1) Background: Conventional transarterial chemoembolization (cTACE) is the mainstay treatment for patients with Barcelona Clinic Liver Cancer (BCLC) B-stage hepatocellular carcinoma (HCC). However, BCLC B-stage patients treated with cTACE represent a prognostically heterogeneous population. We aim to develop and validate a lipiodol-deposition-based nomogram for predicting the long-term survival of BCLC B-stage HCC patients after sequential cTACE. (2) Methods: In this retrospective study, 229 intermediate-stage HCC patients from two hospitals were separately allocated to a training cohort (n = 142) and a validation cohort (n = 87); these patients underwent repeated TACE (≥4 TACE sessions) between May 2010 and May 2017. Lipiodol deposition was assessed by semiautomatic volumetric measurement with multidetector computed tomography (MDCT) before cTACE and was characterized by two ordinal levels: ≤50% (low) and >50% (high). A clinical lipiodol deposition nomogram was constructed based on independent risk factors identified by univariate and multivariate Cox regression analyses, and the optimal cutoff points were obtained. Prediction models were assessed by time-dependent receiver-operating characteristic curves, calibration curves, and decision curve analysis. (3) Results: The median number of TACE sessions was five (range, 4–7) in both cohorts. Before the TACE-3 sessions, the newly constructed nomogram based on lipiodol deposition achieved desirable diagnostic performance in the training and validation cohorts with AUCs of 0.72 (95% CI, 0.69–0.74) and 0.71 (95% CI, 0.68–0.73), respectively, and demonstrated higher predictive ability compared with previously published prognostic models (all p < 0.05). The prognostic nomogram obtained good clinical usefulness in predicting the patient outcomes after TACE. (4) Conclusions: Based on each pre-TACE lipiodol deposition, two sessions are recommended before abandoning cTACE or combining treatment for patients with intermediate-stage HCC. Furthermore, the nomogram based on pre-TACE-3 lipiodol deposition can be used to predict the prognoses of patients with BCLC B-stage HCC. [ABSTRACT FROM AUTHOR]